Chapter 19 Infections of the Skin and Eye (2021) PDF

CHAPTER 19 Infections of the Skin and Eye Copyright © 2021 W. W. Norton & Company, Inc. Infections of the Skin and Eye Chapter Objectives ▪ Correlate the anatomy and physiology of the skin and eyes to the infectious processes affecting them. ▪ Describe symptoms that differentiate skin and...

CHAPTER 19 Infections of the Skin and Eye Copyright © 2021 W. W. Norton & Company, Inc. Infections of the Skin and Eye Chapter Objectives ▪ Correlate the anatomy and physiology of the skin and eyes to the infectious processes affecting them. ▪ Describe symptoms that differentiate skin and eye infections caused by viruses from those caused by bacteria and parasites. ▪ Relate pathogenic mechanisms to disease prevention strategies for microbes that infect the skin and eyes. ▪ Connect the physiology of each pathogen with its antimicrobial treatment and preventive modalities. 2 Rash Ruins Vacation ‒ 1 Scenario ▪ Nate, a 69-year-old type 2 diabetic, awoke in his Naples, Italy hotel room with a tingling sensation that extended from his spine to the middle of his rib cage, like a thin, invisible ribbon. Signs and Symptoms ▪ The discomfort increased until the next morning, when it became severe pain. Small blisters revealed themselves along an irritated red swath of skin. The hotel concierge referred Nate to the local doctor. 3 Rash Ruins Vacation ‒ 2 Diagnosis ▪ The Italian doctor diagnosed Nate with St. Anthony’s fire, a disease, the doctor said, caused by the same virus that causes chickenpox. Nate was surprised to learn that the chickenpox virus he had as a small boy had long ago nestled at the root of one of his spinal nerves. It stayed there until this trip, when it began replicating, causing the painful skin eruptions along the route of that nerve (dermatome). 4 Rash Ruins Vacation ‒ 3 Treatment ▪ The doctor prescribed antiviral and pain relief medications and told Nate to get plenty of rest and make sure that his blood sugar levels were well controlled. He advised Nate to follow up with his regular physician when back in the States. 5 Rash Ruins Vacation ‒ 4 Follow-Up ▪ Nate cut short his trip to Italy and returned home to the United States, where his doctor confirmed the diagnosis and the treatment plan. His doctor told Nate that in Italy, St. Anthony’s fire is another name for shingles, a disease caused by the same virus that causes chickenpox. Resolution ▪ Nate eventually recovered from shingles with the help of his antiviral medication and rest, and he was finally able to return to Italy for a trip that turned out very nicely this time. 6 19.1 Anatomy of the Skin and Eye ‒ 1 Section Objectives ▪ List the different cell components of the skin and their functions. ▪ Describe the structural similarities and differences between dermis and epidermis. ▪ Describe the role of different components of the skin in disease prevention. ▪ Distinguish between the internal and external parts of the eye. 7 19.1 Anatomy of the Skin and Eye ‒ 2 ▪ The skin is the largest human organ, covering, on average, 16–22 square feet of surface. It serves as an effective barrier for blocking microbial access to deeper tissues. 8 Structure of the Skin – 1 ▪ Superficial layer (epidermis) Five layers Dead keratinocytes – Keratin ▪ Deep layer (dermis) Connective tissue Cells Blood vessels, nerves, hair follicles, sweat glands 9 Structure of the Skin – 2 10 What Is a Rash? – 1 ▪ Skin rash Change in color and texture of the skin – Exanthem: widespread skin rash accompanied by systemic symptoms (fever, malaise, headache) – Enanthem: rash on mucous membranes Caused by an infectious agent – A reaction to a toxin produced by o the organism o damage to the skin by the organism o an immune response 11 What Is a Rash – 2 ▪ Different types of rashes Macular: flat and red, less than 1 cm in diameter Papular: small, solid, and elevated Pustular: a papule filled with pus Maculopapular: a papule that is reddened Vesicular: small blisters are formed 12 Mucous Membranes ▪ Mucous membranes (called mucosae; singular, mucosa) Epithelial Serve as barrier (protection) Line the inside of the body Continuous with the skin in several places 13 Structure of the Eye – 1 ▪ External Eyelids Cornea Lens Iris Pupil Sclera ▪ Internal Retina Macula Vitreous humor 14 Structure of the Eye – 2 15 19.2 Viral Infections of the Skin Section Objectives ▪ Classify viruses that cause skin rashes on the basis of their genomic structure. ▪ Explain the pathogenesis of viral skin infection sequelae. ▪ Outline how to diagnose the causative agent of a viral skin infection according to the patient’s signs and symptoms. ▪ Recommend treatment and prevention options for different viral skin infections. 16 Case History: Moyo’s Macular Rash ‒ 1 ▪ Assaggi, a young mother from Mudzengerere village, Zimbabwe, carried her young son, Moyo, 2 miles to the Mosomo clinic. When Moyo arrived, he appeared confused and nonresponsive. He had a high fever and even seized once during the examination. The clinic doctor diagnosed probable viral encephalitis. The physician, noticing that Moyo had a macular rash over much of his body, asked Assaggi whether Moyo had ever been vaccinated for measles. She was evasive at first but finally admitted that her son had not been vaccinated. 17 Case History: Moyo’s Macular Rash ‒ 2 ▪ The clinic doctor had been seeing many cases of measles recently, and a significant number of the affected children had died. He heard that the death toll from the measles epidemic in Zimbabwe stood at 570, 5% of all suspected cases. He started Moyo on the antiviral medication ribavarin but he was not optimistic. A week later Moyo was dead. ▪ Mr. Fibion Rupiya, the village elder, sought assistance from the police and health officials after realizing that several children who recently died had symptoms of measles. The children belonged to a religious sect that disdained immunization. As a result of Mr. Rupiya’s alert, more than 100 children in Mashonaland Central Province were forcibly vaccinated against measles. Some children were locked up in bedrooms by their parents, and others were hidden in the bush, but health officials managed to find the children and vaccinate them. 18 Viruses That Produce Macular Rashes – 1 ▪ Measles (rubeola) Negative-sense, single-stranded RNA virus Very contagious (8‒10 day incubation period) Portal of entry is respiratory or conjunctiva Replicates in the lungs – Moves to regional lymph nodes – Produces a viremia that spreads throughout the body Prodromal period starts with cold/flu-like symptoms. High fever (40°C/104°F) Koplik’s spots – White spots on the buccal mucosa – On inner cheeks 19 Viruses That Produce Macular Rashes – 2 ▪ Measles (rubeola) Immunocompromised patients can develop serious complications – Death – Blindness (ulceration of the cornea) – Myocarditis or pericarditis – Variety of GI maladies Serious complications include – Acute disseminated encephalomyelitis (ADEM) – A delayed complication called subacute sclerosing panencephalitis (SSPE) ADEM is an autoimmune disease that presents during the recovery phase, while SSPE is a progressive degenerative disease of the CNS that occurs 7–10 years after natural measles infection. 20 Viruses That Produce Macular Rashes – 7 21 Viruses That Produce Papular and Pustular Rashes – 1 ▪ Chickenpox Herpesviridae family Varicella-Zoster virus (VZV) Initial exposure = chickenpox – Virus remains latent in the dorsal root ganglia. – Re-emerges later in life in about 20% of patients, which causes shingles Shingles occurs more frequently in older individuals. – Cell-mediated immunity decreases. Chickenpox and shingles are usually diagnosed clinically, but antibody and DNA tests can also be used to detect the virus. 22 Viruses That Produce Papular and Pustular Rashes – 2 ▪ Chickenpox Inhalation of infected particles from skin lesions – Virus replicates in the nasopharynx and infects the regional lymph nodes, leading to viremia. – Second round of viral replication takes place in the liver and spleen. o Followed by a secondary viremia 14–16 days postinfection VZV invades capillary endothelial cells and the deepest layer of the epidermis. – Produces fluid accumulation and vesicle formation Children do not usually have prodromal symptoms and first come down with itchy rash on the face, back, chest, and belly that includes maculopapules, vesicles, pustules, and scabs. 23 Viruses That Produce Papular and Pustular Rashes – 3 ▪ Chickenpox Can be life-threatening in immunocompromised patients Latency – Established when viral DNA integrates into host DNA – Can last for decades – Virus infects the nerve endings of the skin. – Travel along nerves to ganglia where they lie in a dormant state – Latent virus reactivation o Virus particles travel along the sensory nerves of the skin to produce a localized, painful, dermatomal rash known as shingles. 24 Viruses That Produce Papular and Pustular Rashes – 4 ▪ Chickenpox treatment Treated with antihistamines, oatmeal baths, and calamine lotion – Goal is to reduce and control the intense itching and use acetaminophen to reduce pain and fever. Acyclovir is used to treat shingles. – Used only for severe or complicated cases of chickenpox Varicella vaccination – Routine childhood immunization schedule – Varicella vaccine is a live, attenuated form of VZV. Persons 60 years and older should be vaccinated with the zoster vaccine to prevent shingles. 25 Viruses That Produce Papular and Pustular Rashes – 5 ▪ Cold sores and genital herpes Herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) Infects skin and mucous membranes – Able to infect the central nervous system – Occasionally can infect the visceral organs Transmitted by direct contact and replicates in mucosal surfaces or epidermis – Final destination is the neuronal cell in the ganglia, where the virus becomes latent Primary infection may be subclinical or symptomatic. Reactivation of the latent virus always results in symptoms. 26 Viruses That Produce Papular and Pustular Rashes – 6 ▪ Cold sores and genital herpes Severity and recurrence of infection with either virus is dictated by the immune status of the person infected. Cold sores (fever blisters, herpes labialis) – Primarily caused by HSV-1 – HSV-1 is very contagious. – Is present in the active or latent form in 60‒90% of older adults No vaccine against HSV-1 Spread from person to person by contact 27 Viruses That Produce Papular and Pustular Rashes – 7 ▪ Cold sores and genital herpes Primary infections with HSV-1 – Fever, sore throat, muscle aches, and cervical lymphadenopathy, along with vesicular lesions, lasting up to 2 weeks Some patients experience prodromal symptoms such as pain, tingling, or burning sensations before an outbreak. Vesicles commonly form at the outer border of the lips. – Virus present in these lesions can also infect other parts of the body where the skin is disrupted. 28 Viruses That Produce Papular and Pustular Rashes – 8 ▪ Cold sores and genital herpes In children and some health care professionals, abrasions of the skin of the fingers result in an HSV-1 infection called herpetic whitlow. Rugby players and wrestlers also get outbreaks of HSV-1 on the neck, face, and arm called herpes gladiatorum. HSV-1 can set up a chronic infection that involves the deeper parts of the skin in immunocompromised patients. Herpetic keratitis can also affect the cornea. 29 Viruses That Produce Papular and Pustular Rashes – 9 ▪ Cold sores and genital herpes treatment Antiviral medications – Acyclovir, valacyclovir, and famciclovir used during primary infections – Reduce pain and duration of lesions – Decrease viral shedding – Reactivation can be treated with a topical antiviral. HSV-2 causes primarily genital herpes. – Sexually transmitted disease Tissue distribution of HSV-1 and HSV-2 is not absolute. – Possible for HSV-1 to infect the genital skin and mucosa and for HSV-2 to infect the oral tissue 30 Viruses That Produce Papular and Pustular Rashes – 12 ▪ Smallpox (variola) Only known reservoir is humans Eradicated from population in 1979 Member of the Poxviridae family Virus is divided into two variants: – Variola major – Variola minor The variants are very similar to each other and to another virus called the vaccinia virus (cowpox). – Was used to make a vaccine against smallpox 31 Viruses That Produce Papular and Pustular Rashes – 13 ▪ Smallpox (variola) Transmitted by direct or indirect contact o Happens when a person inhales small aerosolized particles or handles fomites containing the virus Virus replicates in the lymph nodes and lymphoid organs; through two sequential viremias, infects internal organs and bone marrow, showing up as – Small spots on the oral mucosa (enanthem) – The pox pustule on the skin (exanthem) 32 Viruses That Produce Papular and Pustular Rashes – 14 ▪ Smallpox (variola) treatment/prevention Diagnosis can be made based on viral cultures and serology No FDA approved treatments for smallpox We no longer vaccinate against smallpox. – Government officials have stockpiled vaccine in strategic centers all across the United States. 33 19.3 Bacterial Infections of the Skin Section Objectives ▪ Name the bacterial pathogens that cause common skin infections. ▪ Categorize skin infections by the physiology of the bacteria causing them. ▪ List clinical and laboratory means of diagnosing bacterial skin infections. ▪ Develop a prevention and treatment plan for bacterial skin infections. 34 Staphylococcal Skin Infections – 1 ▪ Staphylococci associated with skin infections include Staphylococcus epidermidis Staphylococcus aureus – Normal inhabitant of the nares (nose) – Can infect a cut and gain access to the dermis via a hair follicle 35 Staphylococcal Skin Infections – 2 ▪ S. aureus possesses enzymes that contribute to disease. Coagulase coats the bacteria with fibrin and walls off the infection from the immune system and antibiotics, promoting abscess formation. ▪ Staph infections routinely require surgical drainage and antibiotic therapy. ▪ Exotoxins damage host tissue and weaken host defenses. Toxic shock syndrome toxin (TSST): superantigen causes toxic shock syndrome. Exfoliative toxin: superantigen causes a blistering condition in children called scalded-skin syndrome. 36 Staphylococcal Skin Infections – 3 ▪ Staphylococcal skin infections S. aureus infection of hair follicles can be superficial or deep resulting in: – Folliculitis (superficial) – Boil or furuncle (deep) o Carbuncles are boils joined together. 37 Staphylococcal Skin Infections – 4 ▪ Methicillin-resistant S. aureus (MRSA) Strain that has emerged over the past decade Resistant to the antibiotic methicillin – Interfering with cell wall synthesis S. aureus strains (~60%) have now evolved to resist methicillin. ▪ Vancomycin is the treatment of choice. ▪ First appeared as nosocomial infections ▪ Today, MRSA is no longer confined to the hospital. Individuals who have not been in a hospital are being infected with MRSA in what are being called “community acquired infections” at an epidemic rate in the United States. 38 Case History: Leili’s Crusted Lip ‒ 1 ▪ Leili, a 3-year-old girl, was brought to the pediatrician by her mother, who was worried about the rash on Leili’s lip. It started 4 days earlier as a little bump above her lip that spread to the corner of her mouth. The base of the rash was red and covered by pustules. The little girl said that her rash hurt, and the clinician noticed a honey-colored crust on the ruptured pustules. ▪ Leili’s mother said her daughter had not been trying to scratch the rash nor was the area around it hot to the touch. Leili’s mother was told that her little girl had impetigo, a skin infection often caused by bacteria called staphylococci, although streptococci can also cause it. The doctor gently swabbed a sample from one of Leili’s sores and sent it to the lab, where the causative agent would be identified and its antibiotic susceptibility determined. She explained that impetigo is a very contagious disease and she gave Leili’s mother a topical antibiotic to use. 39 Case History: Leili’s Crusted Lip ‒ 2 ▪ Treating topically rather than orally would accomplish two goals. Topical application would reduce the chances that the bacteria would develop drug resistance, and because Leili had a very mild case of impetigo, the antibiotic in the gel should easily penetrate the pustules and kill the organism. Leili and her mother left but returned in a week for a follow-up exam. The “rash” was gone, replaced by Leili’s smile. The pediatrician explained that the cause was in fact methicillin-sensitive Staphylococcus aureus (MSSA), not MRSA. Leili’s mother in turn reported that another child at Leili’s day care had impetigo before Leili, and that is where Leili probably acquired the infection. 40 Staphylococcal Skin Infections – 5 ▪ Impetigo S. aureus and group A strep Two main types of impetigo – Nonbullous o Starts as a superficial bump that becomes a papule and vesicle before it forms the characteristic pustules on erythematous skin o Fluid from the pustules leaks out as they break open (“weeps”). – Bullous o Vesicles grow larger and become bullae that are full of clear yellow fluid. 41 Case History: The Voracious Bacteria ‒ 1 ▪ One weekend in June, Cassi was camping with her three children. She suffered a minor cut on her finger, which she bandaged properly. She also injured the left side of her body while playing sports with her kids. Not thinking much of either of her minor injuries, she went to bed. Two days later, Cassi was extremely ill. Her symptoms included vomiting, diarrhea, and a fever. She was also in severe pain where she had injured her side, and the area had begun to bruise (the skin did not look broken). 42 Case History: The Voracious Bacteria ‒ 2 ▪ By the next day, she could barely get out of bed, and by the end of the night she was breathing with difficulty and could not see. Her side began to leak fluid and blood. Cassi was admitted to the hospital in septic shock, with no detectable blood pressure. She was given vasopressors (medications that constrict the blood vessels) to raise her blood pressure to the normal level. An infectious disease specialist diagnosed the problem as necrotizing fasciitis, and Cassi was rushed into surgery. 43 Case History: The Voracious Bacteria ‒ 3 ▪ In an effort to save her life, about 7% of her body surface was removed. Because the large wound infection in her side would need to resolve before a skin graft could be performed to repair it, the hole in Cassi’s body was left wide open. Meanwhile, the continued use of vasopressors caused gangrene in her fingers and lower extremities. After nearly 3 months and several operations, including amputation, Cassi recovered. 44 Streptococcal Skin Infections – 1 ▪ Streptococcus pyogenes The human nasopharynx and parts of the skin are the natural reservoir for S. pyogenes. ▪ Necrotizing fasciitis, also known as flesh-eating disease Type 1: polymicrobial Type 2: one microorganism, usually S. pyogenes and sometimes S. aureus. Other organisms that can cause necrotizing fasciitis include Clostridium perfringens and Vibrio vulnificus. Therapy includes antibiotics: clindamycin, metronidazole, and gentamicin. ▪ The incidence of necrotizing fasciitis has risen recently due to an increase in the use of NSAIDs, which accentuate a person’s susceptibility to infection by S. pyogenes. 45 Streptococcal Skin Infections – 2 ▪ S. pyogenes virulence factors Capsule: helps organism avoid phagocytosis Pilus-like M protein: binds complement regulatory protein (factor H) Lipoteichoic acid: cell wall component that facilitates adherence to host cells Streptolysins: lyse blood cells Enzymes that degrade – DNA (DNAses), fibrin (streptokinase), and connective tissue (hyaluronidase), making pus less viscous Peptidoglycan: activates the alternative complement pathway and a MAMP that binds NOD-like receptors, causing inflammation 46 Streptococcal Skin Infections – 3 ▪ Exotoxins Streptococcal pyogenic exotoxins (SPEs): superantigens; massive amounts of cytokines released in response to SPEs can produce high levels of inflammation and lead to shock. SPEs are associated with scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis. ▪ Hemolysin Lyses RBCs These streptococci are subclassified into groups A–O according to cell wall antigens. S. pyogenes is the main pathogen among the group A streptococci (GAS). 47 Streptococcal Skin Infections – 4 ▪ Rheumatic fever Can develop after the resolution of a primary GAS infection Sequela is the result of immunological cross-reactivity between specific GAS M protein antigens and host antigens. ▪ Autoreactive B cells activated by the bacterial M protein antigen Make antibodies against cardiac antigen Trigger an inflammatory reaction that damages those tissues 48 Streptococcal Skin Infections – 7 ▪ Acne vulgaris Affects 60–70% of Americans at some point 20% will have severe acne Results from blocked hair follicles or pores called comedones – Can be open (blackheads) – Or closed (whiteheads) Inflammatory acne – Inflamed macules, papules, pustules, and nodules Cystic or nodular acne – Most severe – Painful fluid-filled cysts or nodules 49 Streptococcal Skin Infections – 8 ▪ Acne vulgaris Factors that contribute to acne development are – Genetic predisposition – Hormones – Gram-positive bacterium Propionibacterium acnes o Organism uses the triglycerides in sebum as a nutrient. P. acnes promotes inflammation by binding to Toll-like receptor 2 on macrophages and neutrophils, which then release proinflammatory cytokines. 50 19.4 Fungal Infections of the Skin ‒ 1 Section Objectives ▪ Outline common fungal skin infections according to their etiology. ▪ Compare dermatophytes with other fungi that commonly infect the skin. ▪ Explain how common fungal infections are diagnosed clinically. 51 19.4 Fungal Infections of the Skin ‒ 2 ▪ Fungi Includes molds and yeasts Eukaryotic microbe Filamentous or single-celled ▪ Dermatophytes “love” human skin Cool, moist, keratinized tissues (skin, hair follicles, nails) Epidermophyton, Trichophyton, and Microsporum cause the majority of infections ▪ Named after location in the body Tinea capitis (scalp) Tinea corporis (body) Tinea cruris (jock itch) Tinea pedis (foot) Tinea unguium (nails) 52 19.4 Fungal Infections of the Skin ‒ 3 ▪ Tinea capitis Fungal infection of the scalp Primarily in small children Two varieties: – Black dot tinea capitis (BDTC) – Gray patch tinea capitis (GPTC) ▪ Tinea corporis Ringworm on the body surface, excluding the groin Lesion is round or ring-shaped and itches Ring expands as the fungus grows outward from the initial site of infection 53 19.4 Fungal Infections of the Skin ‒ 4 ▪ Tinea versicolor Long-term (chronic) infection of the skin Prevalent mostly in warm, moist climates Caused by a yeast of the genus Malassezia – Not a dermatophyte Malassezia is a dimorphic yeast. – Can have both yeast and mycelial (hyphal) forms Pathogenesis: round yeast converts to hyphal form. – Invades the stratum corneum Lesions of tinea versicolor are small with a sharp border and hypopigmented skin. – Caused by damage to the melanocytes 54 19.4 Fungal Infections of the Skin ‒ 5 ▪ Candida Candida species – Dimorphic yeasts – Part of the normal flora of the GI tract, vaginal tract, oral cavity, and skin Candida albicans can infect: – The skin (in its mycelial form) – Mucous membranes – Body organs Candida can infect areas where the skin touches and rubs together such as between the fingers, under the arm, or the groin. The most common of these infections is called candidal intertrigo. 55 19.4 Fungal Infections of the Skin ‒ 6 ▪ Fungal skin infections are diagnosed via Clinical appearance Microscopic examination of potassium hydroxide (KOH) preparations of skin flakes or hair – The KOH destroys the skin cells but not the more resilient walls of mycelia or spores, which can be seen under a light microscope. ▪ Fungi can also be cultured on a special selective medium called Sabouraud agar. ▪ Antifungal medications are used to treat these diseases. Imidazole compounds such as clotrimazole are most common and can be purchased over the counter. 56 19.5 Skin Infections of Special Circumstance ▪ Not included 57 19.6 Eye Infections ‒ 1 Section Objectives ▪ Identify viral, bacterial, and fungal causes of eye infections. ▪ Describe the symptoms and etiologies of pink eye. ▪ Explain how the pathogenesis of infectious keratitis differs from that of endophthalmitis. ▪ Outline the relationship between corneal epithelium and fungal keratitis. 58 19.6 Eye Infections ‒ 2 ▪ Eye infections Conjunctivitis – “Pink eye” – Inflammation of the conjunctiva – Can be due to infection, trauma, or an allergic reaction Keratitis – Inflammation of the cornea – Corneal destruction by a bacterial infection Endophthalmitis – Infection of inner structures – Uncommon and almost always results from direct spread of a superficial eye infection or seeding the infection with bacteria carried by blood 59 19.6 Eye Infections ‒ 3 60 Viral Eye Infections – 1 ▪ Herpes viruses Major cause of keratitis and keratoconjunctivitis Herpes Simplex 1 responsible for the majority of cases ▪ Primary lesion may not cause much damage but reactivation of the virus can cause corneal scarring and blindness. ▪ Antiviral medications Acyclovir and trifluridine 61 Viral Eye Infections – 2 ▪ Herpes zoster ophthalmicus Outbreak of shingles along the ophthalmic division of the trigeminal nerve Results in eruption of vesicular lesions on the forehead, eyelids, nose, and may even spread to the eye itself Causes corneal inflammation, eye pain, and sensitivity Treated with oral medications such as acyclovir, valacyclovir, and famciclovir 62 Bacterial Eye Infections – 1 ▪ Bacterial conjunctivitis Affects one eye and is acute, painful, and purulent Pyogenic bacteria such as staph and strep cause marked irritation and a stringy, opaque, grayish or yellowish mucopurulent discharge that may cause the lids to stick together. Chlamydia trachomatis and Neisseria gonorrheae – Cause serious infections of the reproductive system; also cause the majority of acute bacterial conjunctivitis 63 Bacterial Eye Infections – 2 ▪ Chlamydia trachomatis Obligate intracellular bacterial pathogen Inclusion conjunctivitis – Can be contracted by newborns passing through an infected vagina – Prevented prophylactically by treating all newborns with antibiotic eyedrops (erythromycin) Trachoma – Most frequent cause of infectious blindness in the world – Spread by direct contact with eye, nose, and throat secretions – Conjunctiva of the inner eyelid becomes pebbled and causes turning in of the eyelashes (trichiasis). o Eyelashes rake across the cornea, which becomes ulcerated and scarred. Treatment is oral azithromycin and topical tetracycline. 64 Bacterial Eye Infections – 3 ▪ Neisseria gonorrheae Can cause a serious eye disease of infants called ophthalmia neonatorum Organism is passed from an infected mother to newborn during passage through the birth canal. Prophylactic treatment with erythromycin eye drops 65 Fungal and Parasitic Eye Infections – 1 ▪ Fungi and parasites usually have a very hard time infecting the eye. Cannot penetrate the intact corneal epithelium A small injury to the eye can provide opportunity to cause ocular infections. – Wearing a contact lens or getting a foreign body in the eye may cause such an abrasion. 66 Fungal and Parasitic Eye Infections – 2 ▪ Fungal keratitis Caused by species of Fusarium, Aspergillus (both found in the environment), and Candida (part of the normal flora) Diagnosis is made by – Culturing the fungi from a corneal scraping specimen – PCR amplification – Confocal microscopy Invasive lesions require systemic therapy. Superficial lesions treated with Natamycin or Amphotericin B 67 Fungal and Parasitic Eye Infections – 3 ▪ Parasitic keratitis Due to Acanthamoeba species Protozoa that are found ubiquitously in nature (air, water, and soil); in heating, ventilation, and air-conditioning equipment; and even in sewage systems The parasite can exist as a cyst for years when conditions are unfavorable. Ocular Acanthamoeba – Infection makes the eye red, painful, and teary. – Patient will avoid light and suffer visual loss. – If untreated, the effects can be permanent. Acanthamoeba is becoming an increasingly important cause of keratitis in non‒contact lens wearers, but wearing contact lenses remains the primary risk factor. Diagnosis can be difficult, and prolonged treatment is required. 68 Fungal and Parasitic Eye Infections – 4 69 Watch- Protect your eyes  Chapter 19 Animation Varicella-Zoster Virus (VZV) 71 A child is in the hospital diagnosed with staphylococcal scalded skin syndrome (SSSS). Microbiological culture of the blister fluid does not grow any organism. Why were no organisms found? A child is in the hospital diagnosed with staphylococcal scalded skin syndrome (SSSS). Microbiological culture of the blister fluid does not grow any organism. Why were no organisms found? The initial diagnosis is correct. The blisters of SSSS are caused by the toxic shock syndrome toxin (TSST) produced by Staphylococcus aureus. The toxin is secreted by staph that has caused an infection elsewhere in the body and disseminates hematogenously to the skin from that site, so the organisms are not found in the blisters. Question 2 A patient presents with cellulitis caused by Gram-positive cocci that grow in chains. The bacterium is encapsulated and contains the M protein on its surface. What is the most likely identity of the bacterium? a. Staphylococcus aureus b. Streptococcus pyogenes c. Candida albicans d. Propionibacterium acnes 74 Question 2 – Answer A patient presents with cellulitis caused by Gram-positive cocci that grow in chains. The bacterium is encapsulated and contains the M protein on its surface. What is the most likely identity of the bacterium? a. Staphylococcus aureus b. Streptococcus pyogenes c. Candida albicans d. Propionibacterium acnes 75 Clicker Question 3 Which of the following viral infections can be passed across the placenta to a developing fetus? a. rubella b. roseola c. herpes simplex 1 d. rubeola e. varicella-zoster 76 Clicker Question 3 – Answer Which of the following viral infections can be passed across the placenta to a developing fetus? a. rubella b. roseola c. herpes simplex 1 d. rubeola e. varicella-zoster 77 This concludes the Lecture PowerPoint presentation for Chapter 19. For more resources, please visit https://stg-iig.wwnorton.com/michum2/full